Evidence map›Paper›PMID 19806612›Full record

ArticleThe Journal of pathology2010

PAX5 activates the transcription of the human telomerase reverse transcriptase gene in B cells.

Stéphanie Bougel, Stéphanie Renaud, Richard Braunschweig, Dmitri Loukinov, Herbert C Morse, Fred T Bosman, Victor Lobanenkov, Jean Benhattar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Stéphanie BougelInstitute of Pathology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, CH-1011 Lausanne, Switzerland.
Stéphanie Renaud
Richard Braunschweig
Dmitri Loukinov
Herbert C Morse
Fred T Bosman
Victor Lobanenkov
Jean Benhattar
National Institutes of Health · USUniversity Hospital of Lausanne · CHUniversity of Lausanne · CHNational Institute of Allergy and Infectious Diseases · US

Funding

Normal and Pathologic Functions of CTCF and Its Distinct Classes of DNA-targetsZIAAI000860 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LOBANENKOV, VICTOR · 2009 to 2025
$15.4M
Regulation of CTCF Functions and Target Sites by Cancer/Testis-specific CTCF Like BORIS FactorZIAAI001021 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LOBANENKOV, VICTOR · 2009 to 2025
$12.7M
Molecular Regulation of B-Cell Differentiation and FunctionZIAAI001024 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$8.3M
Lymphomas And Retroviral PathogenesisZIAAI000858 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$5.3M
Molecular Mechanisms in Innate immunityZIAAI001057 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$4.7M
Transcriptional Regulation Of Ctcf And Boris ExpressionZ01AI000860 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI LOBANENKOV, VICTOR · 2000 to 2008
$1.5M
Intramural NIH HHS Z01 AI000860Intramural NIH HHS Z99 AI999999Intramural NIH HHS ZIA AI000860Intramural NIH HHS ZIA AI001021Intramural NIH HHS ZIA AI001024Intramural NIH HHS ZIA AI001057NIAID NIH HHS Y99 AI999999
6 · The paper itself

Abstract

Telomerase is an RNA-dependent DNA polymerase that synthesizes telomeric DNA. Its activity is not detectable in most somatic cells but it is reactivated during tumorigenesis. In most cancers, the combination of hTERT hypermethylation and hypomethylation of a short promoter region is permissive for low-level hTERT transcription. Activated and malignant lymphocytes express high telomerase activity, through a mechanism that seems methylation-independent. The aim of this study was to determine which mechanism is involved in the enhanced expression of hTERT in lymphoid cells. Our data confirm that in B cells, some T cell lymphomas and non-neoplastic lymph nodes, the hTERT promoter is unmethylated. Binding sites for the B cell-specific transcription factor PAX5 were identified downstream of the ATG translational start site through EMSA and ChIP experiments. ChIP assays indicated that the transcriptional activation of hTERT by PAX5 does not involve repression of CTCF binding. In a B cell lymphoma cell line, siRNA-induced knockdown of PAX5 expression repressed hTERT transcription. Moreover, ectopic expression of PAX5 in a telomerase-negative normal fibroblast cell line was found to be sufficient to activate hTERT expression. These data show that activation of hTERT in telomerase-positive B cells is due to a methylation-independent mechanism in which PAX5 plays an important role.

Indexed as

Base SequenceBinding, CompetitiveBinding SitesB-LymphocytesCCCTC-Binding FactorCpG IslandsDNA MethylationDNA, NeoplasmGene Expression Regulation, NeoplasticHumansLymphomaMolecular Sequence DataNeoplasm ProteinsPAX5 Transcription FactorPromoter Regions, GeneticRepressor ProteinsCCCTC-Binding FactorCTCF protein, humanDNA, NeoplasmNeoplasm ProteinsPAX5 protein, humanPAX5 Transcription FactorRepressor ProteinsRNA, MessengerRNA, NeoplasmRNA, Small InterferingTelomeraseTERT protein, human

Identifiers

PMID19806612
PMCPMC3422366
OpenAlexW2145258505

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.